title: Relationship between neural alteration and perineural invasion in pancreatic cancer patients with hyperglycemia.
abstract: BACKGROUND
  Patients with higher levels of fasting serum glucose have higher death rates from pancreatic cancer compared to patients with lower levels of fasting serum glucose. However, the reasons have not been studied. The goal of the current study was to examine the neural alterations in pancreatic cancer patients with hyperglycemia and to identify the relationship between the neural alterations and perineural invasion.
  
  
  RESULTS
  The clinical and pathological features of 61 formalin-fixed pancreatic cancer specimens and 10 normal pancreases as controls were analyzed. Furthermore, the expression of Protein Gene Product 9.5 (PGP9.5), Myelin P0 protein (MPP), NGF, TrkA, and p75 were examined by immunohistochemistry. The median number of nerves, the median area of neural tissue, and the median nerve diameter per 10 mm(2) were larger in the hyperglycemia group than those in the euglycemia group (p = 0.007, p = 0.009, and p = 0.004, respectively). The integrated optical density (IOD) of MPP staining was lower in the hyperglycemia group than those in the euglycemia group (p = 0.019), while the expression levels of NGF and p75 were higher in the hyperglycemia group than those in the euglycemia group (p = 0.002, and p = 0.026, respectively). The nerve bundle invasion of pancreatic cancer was more frequent in the hyperglycemia group than in the euglycemia group (p = 0.000).
  
  
  CONCLUSIONS
  Nerve damage and regeneration occur simultaneously in the tumor microenvironment of pancreatic cancer patients with hyperglycemia; the simultaneous occurrence may aggravate the process of perineural invasion. The abnormal expression of NGF and p75 may also be involved in this process and subsequently lead to a lower rate of curative surgery.
authors.affiliation: Department of Hepatobiliary Surgery, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
authors.forename: Junhui
authors.initials: J
authors.lastname: Li
authors.forename: Qingyong
authors.initials: Q
authors.lastname: Ma
authors.forename: Han
authors.initials: H
authors.lastname: Liu
authors.forename: Kun
authors.initials: K
authors.lastname: Guo
authors.forename: Feng
authors.initials: F
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Liang
authors.initials: L
authors.lastname: Han
authors.forename: Fengfei
authors.initials: F
authors.lastname: Wang
authors.forename: Erxi
authors.initials: E
authors.lastname: Wu
mesh_terms: D001786:Blood Glucose / Q000378:metabolism / Q000502:physiology; D021441:Carcinoma, Pancreatic Ductal / Q000097:blood / Q000150:complications* / Q000473:pathology*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000150:complications* / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D009380:Neoplasms, Nerve Tissue / Q000097:blood / Q000378:metabolism / Q000556:secondary; D010179:Pancreas / Q000294:innervation / Q000473:pathology; D010190:Pancreatic Neoplasms / Q000097:blood / Q000150:complications* / Q000473:pathology*; D020361:Paraneoplastic Syndromes, Nervous System / Q000097:blood / Q000209:etiology / Q000473:pathology; D010525:Peripheral Nerves / Q000378:metabolism / Q000473:pathology*; D010523:Peripheral Nervous System Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D059016:Tumor Microenvironment / Q000502:physiology
chemical_list: D001786:Blood Glucose